{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent exome‐sequencing studies have revealed de novo mutations in PURA that are associated with severe neurodevelopmental disorders, including epilepsy and encephalopathy as observed in 5q31.3 microdeletion syndrome. In these patients, mutations in PURA lead to significant neurological impairment and developmental delay, while additional trio‐based studies further underscore the link between PURA dysfunction and neurocognitive deficits. Moreover, structural analyses indicate that even conservative missense mutations compromise the folding integrity, RNA binding, or dimerization of PURA, thereby accounting for the full penetrance of PURA syndrome."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in neurodevelopment, PURA functions as a multifaceted regulator of gene expression at both the transcriptional and translational levels. As part of a complex with linker histone H1.2 and other cofactors, PURA contributes to the repression of p53-dependent transcription and modulates pro-apoptotic gene expression. In cardiac myocytes, PURA—as one of the Pur family proteins—binds purine-rich regulatory elements within the alpha-myosin heavy chain gene, attenuating expression through both transcriptional repression and interference with mRNA translation; its interaction with cell cycle regulators such as cyclin A/Cdk2 further underlies its capacity to restrain proliferation by antagonizing E2F-1 activity. These diverse roles are comprehensively reviewed in the literature, which emphasizes PURA’s evolutionary conservation and its broad nucleic acid-binding properties."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nPURA also plays critical roles in immune regulation and cancer biology. In leukocytes, it partners with hnRNP-K to mediate the repression of CD43 while activating the transcription of CD11c and beta2-integrin genes—activities essential for cell adhesion and hypoxia-induced responses. In prostate cancer, loss of nuclear PURA from repressive complexes contributes to androgen receptor overexpression, whereas restoration of PURA levels can temper aberrant proliferation in androgen-independent cells. In the context of HIV-1 infection, PURA interacts with the viral Rev protein and the Rev-responsive element to facilitate the export of unspliced viral RNAs, thereby modulating host susceptibility to infection. Simultaneously, its participation in the dynamics of cytoplasmic stress granules and processing bodies affects mRNA translation in neurodegenerative diseases such as ALS and in esophageal cancer models where, for example, PURA suppresses the translation of IGFBP3. Importantly, in T cells, signaling events that control the phosphorylation state of PURA influence the transcription of cytokines such as interleukin-9, linking PURA to allergic immune responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nRecent investigations further implicate PURA in metabolic regulation and the maintenance of genomic integrity. In esophageal squamous cell carcinoma, PURA binds to specific motifs within the promoter of mitochondrial phosphoenolpyruvate carboxykinase, PCK2, thereby stimulating cellular oxidative phosphorylation and fatty acid metabolism; similar transcriptional activation is observed in the context of CASP8, where PURA forms complexes with E2F-1 and RNA polymerase II. In addition, PURA functions at stalled replication forks and in double-strand break repair, underscoring its involvement in cellular responses to DNA replication stress. Collectively, these studies even highlight microRNA-mediated regulation of PURA—with miR-144 directly targeting its mRNA—which further integrates PURA into oncogenic and metabolic signaling pathways. Lastly, emerging evidence suggests that PURA might also contribute to metastasis in esophageal cancer, a prospect that warrants further exploration."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "24", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Seema R Lalani, Jing Zhang, Christian P Schaaf, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Mutations in PURA cause profound neonatal hypotonia, seizures, and encephalopathy in 5q31.3 microdeletion syndrome."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Am J Hum Genet (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.ajhg.2014.09.014"}], "href": "https://doi.org/10.1016/j.ajhg.2014.09.014"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25439098"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25439098"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Katherine L Helbig, Kelly D Farwell Hagman, Deepali N Shinde, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Diagnostic exome sequencing provides a molecular diagnosis for a significant proportion of patients with epilepsy."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genet Med (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/gim.2015.186"}], "href": "https://doi.org/10.1038/gim.2015.186"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26795593"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26795593"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "David Hunt, Richard J Leventer, Cas Simons, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Whole exome sequencing in family trios reveals de novo mutations in PURA as a cause of severe neurodevelopmental delay and learning disability."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Med Genet (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1136/jmedgenet-2014-102798"}], "href": "https://doi.org/10.1136/jmedgenet-2014-102798"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25342064"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25342064"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Marcel Proske, Robert Janowski, Sabrina Bacher, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Isolation and characterization of a novel H1.2 complex that acts as a repressor of p53-mediated transcription."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M708205200"}], "href": "https://doi.org/10.1074/jbc.M708205200"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18258596"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18258596"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Madhu Gupta, Viranuj Sueblinvong, Jai Raman, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Single-stranded DNA-binding proteins PURalpha and PURbeta bind to a purine-rich negative regulatory element of the alpha-myosin heavy chain gene and control transcriptional and translational regulation of the gene expression. Implications in the repression of alpha-myosin heavy chain during heart failure."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Biol Chem (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1074/jbc.M307696200"}], "href": "https://doi.org/10.1074/jbc.M307696200"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12933792"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12933792"}]}, {"type": "r", "ref": 7, "children": [{"type": "t", "text": "Hong Liu, Sharon M Barr, Caryn Chu, et al. 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